anti-Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila), Translocated To, 3 (MLLT3) Antibodies

Human Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila), Translocated To, 3 (MLLT3) interaction partners

1. miR (show MLXIP Antibodies)-564 inhibited metastasis and proliferation of prostate cancer by targeting MLLT3

2. MLL (show MLL Antibodies)-AF9 fusion is associated with acute myeloid leukemia (show BCL11A Antibodies).

3. Structural insights into H3 histone (show HIST1H3B Antibodies) crotonyl-lysine recognition by the AF9 YEATS domain have been presented.

4. A luciferase reporter gene assay revealed that hsp70 promoter activation is enhanced by the transcriptional co-activator AF9 and splicing mediator SNRPE, but suppressed by the coiled-coil domain-containing protein CCDC127.

5. YEATS domain of AF9 directly links histone crotonylation to active transcription.

6. Results show that human MLL (show MLL Antibodies)-AF9 expression in mouse long-term hematopoietic stem cells causes invasive, chemoresistant acute myeloid leukemia (show BCL11A Antibodies) that expresses genes related to epithelial-mesenchymal transition.

7. Results show that MLL (show MLL Antibodies)-AF9 reduces Id2 and increases E2-2 (show TCF4 Antibodies) expression to drive and sustain leukemia stem cell potential in MLL (show MLL Antibodies)-rearranged acute myeloid leukemia (show BCL11A Antibodies) (AML (show RUNX1 Antibodies)). Low expression of Id2 or of an Id2 gene signature is associated with poor prognosis in not only MLL (show MLL Antibodies)-rearranged but also t(8;21) AML (show RUNX1 Antibodies) patients.

8. Exploring the mechanism how AF9 recognizes and binds H3K9ac by molecular dynamics simulations and free energy calculations.

9. Studies identified the evolutionarily conserved Af9 YEATS domain as a novel acetyllysine-binding module and established a direct link between histone acetylation and DOT1L (show DOT1L Antibodies)-mediated H3K79 methylation in transcription control.

10. AF9 and its homolog ENL directly interact with AF4.

Mouse (Murine) Myeloid/lymphoid Or Mixed-Lineage Leukemia (Trithorax Homolog, Drosophila), Translocated To, 3 (MLLT3) interaction partners

1. Atg5 (show ATG5 Antibodies)-dependent autophagy contributes to the development of acute myeloid leukemia (show BCL11A Antibodies) in an MLL (show MLL Antibodies)-AF9-driven mouse model.

2. YEATS domain of AF9 directly links histone crotonylation to active transcription.

3. Data suggest that RAS-homolog enriched in brain protein (Rheb1) promotes MLL-AF9 fusion protein initiated acute myeloid leukemia (AML) progression through target of rapamycin complex 1 (mTORC1) signaling pathway.

4. Using a PDK1 (show PDPK1 Antibodies) conditional deletion MLL (show MLL Antibodies)-AF9 murine AML (show RUNX1 Antibodies) model, we revealed that the deletion of PDK1 (show PDPK1 Antibodies) prolonged the survival of AML (show RUNX1 Antibodies) mice by inducing LSC (show ARHGEF1 Antibodies) apoptosis

5. define a specific pairing of two amino acids that creates a salt bridge between MLLT1 (show MLLT1 Antibodies)/3 and AFF proteins that is critically important for MLL (show MLL Antibodies)-mediated transformation of HPCs

6. Af9 mediates site-selective physical and functional recruitment of Rnf2 (show RNF2 Antibodies) to the alpha-ENaC (show SCNN1A Antibodies) promoter to constrain basal alpha-ENaC (show SCNN1A Antibodies) transcription in collecting duct cells.

7. Impaired alphaENaC (show SCNN1A Antibodies) expression due to failure to inhibit Dot1a-Af9 may play an important role in the early stages of pseudohypoaldosteronism type 1 in MR(-/-) mice.

8. We demonstrate that leukemogenic activity of MLL (show MLL Antibodies)-AF9 requires RUVBL2 (RuvB-like 2 (show RUVBL2 Antibodies)), an AAA (show AAAS Antibodies)+ ATPase (show DNAH8 Antibodies) family member that functions in a wide range of cellular processes, including chromatin remodeling and transcriptional regulation.

9. Therefore, Dot1a and Af9 as aldosterone-downregulated targets are negative regulators of endothelin-1 (show EDN1 Antibodies) transcription in vitro and in vivo, and may be considered as new potential therapeutic targets of kidney injury in diabetes.

10. It was concluded that +78/+92 of the epithelial Na+ channel alpha (show SCNN1A Antibodies)-subunit (show POLG Antibodies) represents the primary Af9 binding site involved in recruiting Dot1a to repress basal and aldosterone-sensitive Na+ channel alpha-subunit (show POLG Antibodies) transcription.